People who suffer severe burns or comprehensive skin injuries are typically delegated to deal with severe scarring, disfigurement, and skin that feels chronically tight and scratchy.
That’s because the body’s recovery processes have actually evolved to concentrate on avoiding infection by quickly closing up wounds, rather than regrowing or bring back normal skin tissue.
New research study led by Dr. Jeff Biernaskie, PhD, has made an amazing leap forward in comprehending how skin heals, which might result in drug treatments to greatly improve injury healing. The study, published in the clinical journal Cell Stem Cell, was co-led by Dr. Sepideh Abbasi, PhD, Sarthak Sinha, MD/PhD prospect and Dr. Elodie Labit, PhD, postdoctoral fellow.
“We identified a specific population of progenitor cells that reside within the dermis, the deep connective tissue of the skin. Progenitor cells, are unique in that they are able to undergo cell division and generate many new cells to either maintain or repair tissues. Following injury, these dermal progenitors become activated, proliferate and then migrate into the wound where they generate nearly all of the new tissue that will fill the wound, both scar and regenerated tissue,” says Biernaskie, professor of stem cell biology in the University of Calgary Faculty of Veterinary Medicine (UCVM), and the Calgary Firefighters Burn Treatment Society Chair in Skin Regeneration and Wound Healing.
Biernaskie’s extensive study, five years in the making, uses brand-new understanding on why particular dermal cells have the ability to restore brand-new skin, rather than injuring scar tissue. Using innovative genomics techniques to profile thousands of specific cells at various times after injury, the research study group compared scar-forming versus regenerative zones within skin wounds.
“Remarkably, we found that although these cells come from the same cellular origin, different microenvironments within the wound activate entirely different sets of genes. Meaning, the signals found within ‘regenerative zones’ of the wound promote re-activation of genes that are typically engaged during skin development. Whereas, in scar-forming zones these pro-regenerative programs are absent or suppressed and scar-forming programs dominate.”
Dealing with these findings, the scientists then showed it’s possible to modify the hereditary programs that govern skin regeneration.
“What we’ve shown is that you can alter the wound environment with drugs, or modify the genetics of these progenitor cells directly, and both are sufficient to change their behaviour during wound healing. And that can have really quite impressive effects on healing that includes regeneration of new hair follicles, glands and fat within the wounded skin,” says Biernaskie.
This research uses crucial insights into the molecular signals that drive scar formation throughout wound recovery and it identifies a variety of genetic signals that are able to conquer fibrosis and promote real regrowth of adult skin.
“This proof of principle is really important, because it suggests that the adult wound-responsive cells do in fact harbor a latent regenerative capacity, it just simply needs to be unmasked,” says Biernaskie. “Now, we are actively looking for additional pathways that may be involved. Our hope is to develop a cocktail of drugs that we could safely administer in humans and animals to entirely prevent genetic programs that initiate scar formation in order to greatly improve the quality of skin healing.”